Bibliographic Details
| Title: |
Neutrophil-inflicted vasculature damage suppresses immune-mediated optic nerve regeneration |
| Authors: |
Ryan Passino, Matthew C. Finneran, Hannah Hafner, Qian Feng, Lucas D. Huffman, Xiao-Feng Zhao, Craig N. Johnson, Riki Kawaguchi, Juan A. Oses-Prieto, Alma L. Burlingame, Daniel H. Geschwind, Larry I. Benowitz, Roman J. Giger |
| Source: |
Cell Reports, Vol 43, Iss 3, Pp 113931- (2024) |
| Publisher Information: |
Elsevier, 2024. |
| Publication Year: |
2024 |
| Collection: |
LCC:Biology (General) |
| Subject Terms: |
CP: Neuroscience, Biology (General), QH301-705.5 |
| More Details: |
Summary: In adult mammals, injured retinal ganglion cells (RGCs) fail to spontaneously regrow severed axons, resulting in permanent visual deficits. Robust axon growth, however, is observed after intra-ocular injection of particulate β-glucan isolated from yeast. Blood-borne myeloid cells rapidly respond to β-glucan, releasing numerous pro-regenerative factors. Unfortunately, the pro-regenerative effects are undermined by retinal damage inflicted by an overactive immune system. Here, we demonstrate that protection of the inflamed vasculature promotes immune-mediated RGC regeneration. In the absence of microglia, leakiness of the blood-retina barrier increases, pro-inflammatory neutrophils are elevated, and RGC regeneration is reduced. Functional ablation of the complement receptor 3 (CD11b/integrin-αM), but not the complement components C1q−/− or C3−/−, reduces ocular inflammation, protects the blood-retina barrier, and enhances RGC regeneration. Selective targeting of neutrophils with anti-Ly6G does not increase axogenic neutrophils but protects the blood-retina barrier and enhances RGC regeneration. Together, these findings reveal that protection of the inflamed vasculature promotes neuronal regeneration. |
| Document Type: |
article |
| File Description: |
electronic resource |
| Language: |
English |
| ISSN: |
2211-1247 |
| Relation: |
http://www.sciencedirect.com/science/article/pii/S2211124724002596; https://doaj.org/toc/2211-1247 |
| DOI: |
10.1016/j.celrep.2024.113931 |
| Access URL: |
https://doaj.org/article/292ce40fd6534ad8ac191a8ef34cab42 |
| Accession Number: |
edsdoj.292ce40fd6534ad8ac191a8ef34cab42 |
| Database: |
Directory of Open Access Journals |
